Spatiotemporal distribution and pollution assessment of trace metals in the Buriganga River, Bangladesh.

The Buriganga River plays a key role in the socioeconomic structure of Dhaka, the capital of Bangladesh. However, this river is severely polluted and is considered one of the most polluted in the world. Therefore, this study aimed to assess the concentrations of various metals in the Buriganga River. A study was conducted from August 2019 to February 2020 to determine the concentrations of 16 metals in water samples (n = 210) collected from 10 distinct sites in the Buriganga River. The mean values for the concentrations of Cr, Mn, Ni, Zn, As, Se, Cd, Sb, and Pb in river water were above the guideline values prescribed by the WHO, Japan, and Bangladesh. Moreover, the fraction ratios of Be, Cr, Co, Ni, Cu, Zn, Se, Mo, Ag, Cd, Sb, and Pb were high (>0.85); consequently, these metals could accumulate at high concentrations in river sediments. Assessment using the single-factor pollution index allowed the classification of the pollution level as 'serious pollution' for Sb and 'heavy pollution' for Cd, Ni, and Pb. The trace metal concentrations in this river imply that crops cultivated along the river using river water may also be contaminated with trace metals.

Effect of Hand and Foot Massage Therapy on Psychological Factors and EEG Activity in Elderly People Requiring Long-Term Care: A Randomized Cross-Over Study.

Massage therapy is widely used as a complementary therapy in the elderly. Here, we investigate the effect of hand and foot massage therapy on psychological factors and electroencephalographic (EEG) activity in elderly people requiring long-term care. We included 12 elderly people requiring long-term care, who were randomly divided into two groups (A and B). Group A received hand massage and group B received foot massage, both for 15 min each. After 1 week, group A received foot massage and group B received hand massage, both for 15 min each. We assessed emotions and mood states with a Likert scale after each massage and resting-state EEG activity was measured before and after each massage. Our results showed that both hand and foot massage led to a high degree of pleasant, relaxed, and refreshed feelings. Moreover, resting-state alpha activity significantly increased in the left insular cortex after hand massage (p < 0.05), and in the right and left posterior cingulate cortex after foot massage (p < 0.05). This study suggests that hand and foot massage therapy modulate psychological factors and EEG activity in elderly people requiring long-term care.

Aggravating effects of Asian sand dust on lung eosinophilia in mice immunized beforehand by ovalbumin.

Asian sand dust (ASD) event may result in a significant influence on an asthmatic patient. However, for obvious reasons, there is no experimental study in which asthmatic patients are exposed to ASD. This study was undertaken to clarify the effects of ASD on lung eosinophiliain mice immunized beforehand by ovalbumin (OVA). CD-1 mice were instilled intratracheally with OVA four times at 2-week intervals. Simultaneous intratracheal administration of OVA and ASD (OVA + ASD sim) at the last OVA treatment or intratracheal administration with ASD 1 day before (OVA + ASD pre) /after (OVA + ASD post) the last OVA treatment was performed to investigate the effects of OVA and ASD exposure timing. The three kinds of treatment (OVA + ASD pre; OVA + ASD sim; OVA + ASD post) aggravated allergic lung inflammation and proliferation of goblet cells in the airway epithelium in mice, as evidenced by the cellular profile of bronchoalveolar lavage fluid (BALF) and pathological examination. As an overall trend, these changes were paralleled with the expression of Th2-associated effecter molecules and eosinophil relevant cytokine chimokines in BALF as well as the production of OVA-specific IgG1 compared with OVA treatment alone. OVA + ASD sim aggravated lung eosinophilia remarkably compared with the other treatments. The order of the potency of the aggravation was OVA+ASD pre < OVA+ASD post

Asian sand dust enhances murine lung inflammation caused by Klebsiella pneumoniae.

Inhaling concomitants from Asian sand dust (ASD) may result in exacerbation of pneumonia by the pathogen. The exacerbating effect of ASD on pneumonia induced by Klebsiella pneumoniae (KP) was investigated in ICR mice. The organic substances adsorbed onto ASD collected from the atmosphere of Iki-island in Japan were excluded by heat treatment at 360°C for 30min. ICR mice were instilled intratracheally with ASD at doses of 0.05mg or 0.2mg/mouse four times at 2-week intervals (total dose of 0.2mg or 0.8mg/mouse) and were administrated with ASD in the presence or absence of KP at the last intratracheal instillation. Pathologically, ASD caused exacerbation of pneumonia by KP as shown by increased inflammatory cells within the bronchiolar and the alveolar compartments. ASD enhanced the neutrophil number dose dependently as well as the expression of cytokines (IL-1ß, IL-6, IL-12, IFN-γ, TNF-α) and chemokines (KC, MCP-1, MIP-1α) related to KP in BALF. In an in vitro study using RAW264.7 cells, combined treatment of ASD and KP increased gene expression of IL-1ß, IL-6, IFN-ß, KC, MCP-1, and MIP-1α. The same treatment tended to increase the protein level of IL-1ß, TNF-α and MCP-1 in a culture medium compared to each treatment alone. The combined treatment tended to increase the gene expression of Toll-like receptor 2 (TLR2), and NALP3, ASC and caspase-1 compared with KP alone. These results suggest that the exacerbation of pneumonia by ASD+KP was due to the enhanced production of pro-inflammatory mediators via activation of TLR2 and NALP3 inflammasome pathways in alveolar macrophages.

Airborne Asian sand dust enhances murine lung eosinophilia.

There is no experimental study demonstrating the effects of airborne Asian sand dust (AASD) on allergic lung eosinophilia. The organic substances adsorbed onto AASD collected from the atmosphere of Iki-island in Japan were excluded by heat treatment at 360°C for 30 min. The effects of AASD or heated-AASD (H-AASD) towards allergic lung inflammation were compared in murine lungs to investigate the role of organic substances. ICR mice were administrated with the two kinds of AASD and/or ovalbumin (OVA) intratracheally four times at 2-week intervals. AASD and H-AASD enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. AASD and H-AASD synergistically increased Th2 cytokines-interleukin-13 (IL-13), eosinophil-relevant cytokine and chemokine, such as IL-5, and monocyte chemotactic protein-3 (MCP-3) induced by OVA in whole lung lavage fluid. The enhancing effects were much greater in AASD than in H-AASD. AASD induced adjuvant effects on OVA-specific immunoglobulin E (IgE) and IgG1 production. In an in vitro study using RAW264.7 cells, AASD increased the expression of Toll-like receptors 2 (TLR2) mRNA, but not TLR4 mRNA. AASD increased mRNA expression of NALP3, ASC, and IL-1ß compared with the control. H-AASD caused no expression of either mRNA. These results suggest that the aggravated lung eosinophilia in AASD is due to activation of a Th2-associated immune response and that the activation of TLR2 and NALP3 inflammasome by microbial materials could be participating in this phenomenon.

Urban particulate matter in Beijing, China, enhances allergen-induced murine lung eosinophilia.

It has been reported that ambient particulate matter (PM) in some large cities, such as Beijing, China, causes adverse respiratory health effects. However, there is currently no experimental report on the relationship between bronchial asthma and urban PM (UPM) in northeast Asia. In this study, the microbial and chemical substances adsorbed onto UPM collected in Beijing were excluded by heat-treatment at 360 degrees C for 30 min. The effects of UPM or heated UPM (H-UPM) toward allergic lung inflammation were compared in murine lungs to investigate the role of organic substances. ICR mice were administrated intratracheally with the two kinds of UPM and/or ovalbumin (OVA) 4 times at 2-week intervals. UPM and H-UPM enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. UPM and H-UPM synergistically increased Th-2 cytokines--interleukin (IL)-4 and IL-13, eosinophil-relevant cytokines and chemokines, such as IL-5 and monocyte chemotactic protein-3 (MCP-3), induced by OVA in bronchoalveolar lavage fluid (BALF). The enhancing effects were much greater in UPM than in H-UPM. UPM induced adjuvant effects on specific immunoglobulin E (IgE) and IgG1 production by OVA. In an in vitro study using RAW264.7 cells, UPM increased the expression of Toll-like receptor 2 (TLR2) mRNA, but not TLR4 mRNA. H-UPM caused no expression of both TLR mRNAs. These results suggest that the aggravated lung eosinophilia in UPM was due to activation of a Th2-associated immune response via the activation of TLR2 by microbial materials. Chemical materials of air pollutant origin contained in UPM, and inorganic components (elemental carbon, mineral elements) in H-UPM, could also cause the aggravation.

Characterization of NIES CRM No. 23 Tea Leaves II for the determination of multielements.

A candidate environmental certified reference material (CRM) for the determination of multielements in tea leaves and materials of similar matrix, NIES CRM No. 23 Tea Leaves II, has been developed and characterized by the National Institute for Environmental Studies (NIES), Japan. The origin of the material was tea leaves, which were ground, sieved through a 106-microm mesh, homogenized, and then subdivided into amber glass bottles. The results of homogeneity and stability tests indicated that the material was sufficiently homogeneous and stable for use as a reference material. The property values of the material were statistically determined based on chemical analyses by a network of laboratories using a wide range of methods. Sixteen laboratories participated in the characterization, and nine certified values and five reference values were obtained. These property values of the candidate CRM, which are expressed as mass fractions, were close to the median and/or mean values of the mass fractions of elements in various tea products. The candidate CRM is appropriate for use in analytical quality control and in the evaluation of methods used in the analysis of tea and materials of similar matrix.

Asian sand dust aggravates allergic rhinitis in guinea pigs induced by Japanese cedar pollen.

Asian sand dust (ASD) contains microbial materials, sulfate (SO(4)(2-)), and nitrate (NO(3)(-)), and is derived from air pollutants in East China. ASD reportedly causes adverse respiratory health effects; a case in point is aggravated allergen-associated experimental lung eosinophilia. Guinea pigs were administered normal saline (control), ASD (0.3 mg/animal), ASD (0.6 mg/animal), Japanese cedar pollen (JCP) (0.2 mg/kg body weight), JCP + ASD (0.3 mg/animal), or JCP + ASD (0.6 mg/animal), into their nasal cavities at seven weekly intervals. The number of sneezes, amount of nasal secretions, and nasal obstructing response were measured as indices of nasal responses. Total immunoglobulin E (IgE) antibodies in serum and the number of eosinophils, histamine, and arachidonic acid metabolites in nasal cavity lavage fluids (NCLF) were also measured. ASD enhanced the JCP-associated nasal obstructing response, but not the number of sneezes or amount of nasal secretions. ASD enhanced JCP-associated cysteinyl leukotrienes (C(4), D(4), E(4)) and histamine production in NCLF. ASD augmented the number of eosinophils in NCLF and total IgE in serum induced by JCP. ASD enhanced eosinophil recruitment in the nasal mucosa, and goblet cell proliferation in the nasal epithelium induced by JCP. These results suggest that ASD enhances the nasal allergic reaction induced by repeated JCP administration in guinea pigs.

Severe arterial hypertension: a possible complication of McCune-Albright syndrome.

McCune-Albright syndrome is characterized by café-au-lait spot, multiple endocrine hyperfunction, and polyostotic fibrous dysplasia. A somatic point mutation of Gsalpha protein leads to an increase in the Gsalpha-associated hormone activity in McCune-Albright syndrome. Because cyclic adenosine 3',5'-monophosphate stimulates the dopamine beta hydroxylase gene, an activating mutation of the Gsalpha protein may cause the hyperproduction of norepinephrine via dopamine. We report on a 9-year-old girl with McCune-Albright syndrome complicated by severe arterial hypertension. The urinary excretion of norepinephrine was 5- to 10-fold higher than in age-matched controls. Meta-iodobenzylguanidine scintigraphy and positron emission tomography/computed tomography (PET/CT) revealed no hot spots. These findings suggest that severe hypertension might be due to an activating mutation of Gsalpha protein in sympathetic ganglia. Because of the reported association of GNAS1 gene polymorphism with hypertension, our patient provides further evidence for a role of Gsalpha protein in hypertension.

Effects of asian sand dust, Arizona sand dust, amorphous silica and aluminum oxide on allergic inflammation in the murine lung.

The aggravating effects of Asian sand dust (SD) and related minerals on the allergic inflammation were examined in the murine lungs. The toxic materials adsorbed onto Asian SD, Arizona SD were inactivated by heat-treatment. ICR mice were administered mineral samples (0.1 mg/mouse) and/or ovalbumin (OVA) (1 microg/mouse) - normal saline (control), Asian SD, Arizona SD, SiO2, Al2O3, OVA, OVA + Asian SD, OVA + Arizona SD, OVA + SiO2, and OVA + Al2O3 - intratracheally four times at two-week intervals. All samples tested enhanced eosinophil recruitment induced by ovalbumin in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. Arizona SD alone caused a slight increase of neutrophils in bronchoalveolar lavage fluids along with pro-inflammatory mediators, such as keratinocyte chemoattractant, but Asian SD alone or Al2O3 alone showed no effect. The test particles, except Al2O3, synergistically increased the numbers of eosinophils in BALF induced by ovalbumin. In particular, Arizona SD and SiO2 synergistically increased the eosinophil relevant cytokine and chemokine, such as IL-5 and monocyte chemotactic protein (MCP)-3. The aggravating effects of the samples were dependent on the SiO2 content. All samples tested also induced the adjuvant effects to specific IgG1 production by OVA. These results suggest that the aggravated allergic inflammation by mineral dusts may be due to the mineral elements (mainly SiO2). The enhancement by Arizona SD may be mediated, at least partially, by the increased expression of IL-5 and MCP-3 and also by the modulated expression of IL-5 and MCP-3.

Development and certification of the new NIES CRM 28: urban aerosols for the determination of multielements.

A new environmental certified reference material (CRM) for the determination of multielements in aerosol particulate matter has been developed and certified by the National Institute for Environmental Studies (NIES), Japan, based on analyses by a network of laboratories using a wide range of methods. The origin of the material was atmospheric particulate matter collected on filters in a central ventilating system in a building in Beijing city centre. The homogeneity and stability of this material were sufficient for its use as a reference material. Values for elemental mass fractions in the material were statistically determined based on the analytical results of the participating laboratories. Eighteen certified values and 14 reference values were obtained. The diameters, obtained from a micrographic image using image analysis software, of 99% of the particles were less than 10 microm, demonstrating that almost all the particles in the material could be classified as particles of 10 microm or less in aerodynamic diameter. The chemical composition and particle size distribution of this material were close to those of an authentic aerosol collected in Beijing. NIES CRM 28 is appropriate for use in analytical quality control and in the evaluation of methods used in the analysis of aerosols, particularly those collected in urban environments in northeast Asia.

Gene expression analysis of murine lungs following pulmonary exposure to Asian sand dust particles.

The respiratory health impact of Asian sand dust events originating in the deserts of China has become a concern within China and in its neighboring countries. We examined the effects of Asian sand dust particles (ASDPs) on gene expression in the murine lung using microarray analysis and elucidated the components responsible for lung inflammation. Male ICR mice were intratracheally administrated ASDPs, heat-treated ASDPs (ASDP-F, lipopolysaccaride [LPS], or beta-glucan free), or kaolin particles. We performed microarray analysis for murine lungs, the results of which were confirmed by quantitative reverse transcription-polymerase chain reaction (RT-PCR). We also assessed the protein expression and histologic changes. Exposure to ASDP, ASDP-F, or kaolin upregulated (>2-fold) 112, 36, or 9 genes, respectively, compared with vehicle exposure. In particular, ASDP exposure markedly enhanced inflammatory response-related genes, including chemokine (C-X-C motif) ligand 1/keratinocyte-derived chemokine, chemokine (C-X-C motif) ligand 2/macrophage inflammatory protein-2, chemokine (C-C motif) ligand 3/macrophage inflammatory protein-1alpha, and chemokine (C-X-C motif) ligand 10/interferon-gamma-inducible protein-10 (>6-fold). The results were correlated with those of the quantitative RT-PCR and the protein expression analyses in overall trend. In contrast, exposure to ASDP-F attenuated the enhanced expression of these proinflammatory molecules. Kaolin exposure increased the expression of genes and proteins for the chemokines. In histopathologic changes, exposure to ASDP prominently enhanced pulmonary neutrophilic inflammation, followed by kaolin and ASDP-F exposure in the order. Taken together, exposure to ASDP causes pulmonary inflammation via the expression of proinflammatory molecules, which can be attributed to LPS and beta-glucan absorbed in ASDPs. Furthermore, microarray analysis should be effective for identifying potentially novel genes, sensitive biomarkers, and pathways involved in the health effects of the exposure to environmental particles (e.g., ASDPs).

Enhancement of mite allergen-induced eosinophil infiltration in the murine airway and local cytokine/chemokine expression by Asian sand dust.

Data on the effects of sand dust toward allergic asthma produced by indoor allergens, such as house dust mites, are not currently available. This study was undertaken to clarify the role of Asian sand dust on mite allergen, Dermatophagoides farinae (D. farinae)-induced eosinophilic inflammation in the murine lung, using sand dusts from the Maowusu Desert (Inner Mongolia) (SD-1) and the Tengger Desert (China) (SD-2). ICR mice were intratracheally administered saline; SD-1 alone; SD-2 alone; D. farinae alone; D. farinae + SD-1; and D. farinae + SD-2, 4 times at 2-wk intervals. The two sand dusts enhanced infiltration of eosinophil in the airway, along with goblet-cell proliferation related to D. farinae. The degree of eosinophil infiltration induced with SD-2 was greater than with SD-1. The SD-1, which contained higher amounts of beta-glucan, increased the expression of interferon (IFN)-gamma in bronchoalveolar lavage fluids (BALF) with or without D. farinae, but SD-2 did not. Synergistically or cumulatively elevated levels of interleukin (IL)-5, eotaxin, and monocyte chemotactic protein in BALF related to D. farinae were higher with D. farinae + SD-2 than with D. farinae + SD-1. These results suggest that increased cytokine and chemokines in BALF play an important role in the enhancement of eosinophil infiltration in the airway induced by D. farinae + sand dusts. The reduced eosinophil infiltration in the SD-1-treated mice could be due to suppression of Th-2 cytokine and eotaxin via interferon-gamma induced by microbial materials, such as beta-glucan.

Asian sand dust enhances ovalbumin-induced eosinophil recruitment in the alveoli and airway of mice.

Asian sand dust (ASD) containing sulfate (SO4(2-)) reportedly causes adverse respiratory health effects but there is no experimental study showing the effect of ASD toward allergic respiratory diseases. The effects of ASD and ASD plus SO4(2-) toward allergic lung inflammation induced by ovalbumin (OVA) were investigated in this study. ICR mice were administered intratracheally with saline; ASD alone (sample from Shapotou desert); and ASD plus SO4(2-) (ASD-SO4); OVA+ASD; OVA+ASD-SO4. ASD or ASD-SO4 alone caused mild nutrophilic inflammation in the bronchi and alveoli. ASD and ASD-SO4 increased pro-inflammatory mediators, such as Keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-1 alpha, in bronchoalveolar lavage fluids (BALF). ASD and ASD-SO4 enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. However, a further increase of eosinophils by addition of SO4(2-) was not observed. The two sand dusts synergistically increased interleukin-5 (IL-5) and monocyte chemotactic protein-1 (MCP-1), which were associated with OVA, in BALF. However, the increased levels of IL-5 were lower in the OVA+ASD-SO4 group than in the OVA+ASD group. ASD caused the adjuvant effects to specific-IgG1 production by OVA, but not to specific-IgE. These results suggest that the enhancement of eosinophil recruitment in the lung is mediated by synergistically increased IL-5 and MCP-1. IgG1 antibodies may play an important role in the enhancement of allergic reaction caused by OVA and sand dust. However, extra sulfate may not contribute to an increase of eosinophils.

Pulmonary toxicity induced by intratracheal instillation of Asian yellow dust (Kosa) in mice.

Asian yellow dust (Kosa) causes adverse respiratory health effects in humans. The objective of this study was to clarify the lung toxicity of Kosa. ICR mice (5 weeks of age) were administered intratracheally with Kosa samples-two samples from Maowusu desert and Shapotou desert, one sample consisted of Shapotou Kosa plus sulfate, and natural Asian dust (NAD) from the atmosphere of Beijing-at doses of 0.05, 0.10 or 0.20mg/mouse at four weekly intervals. The four Kosa samples tested had similar compositions of minerals and concentrations of elements. Instillation of dust particles caused bronchitis and alveolitis in treated mice. The magnitude of inflammation was much greater in NAD-treated mice than in the other particles tested. Increased neutrophils, lymphocytes or eosinophils in bronchoalveolar lavage fluids (BALF) of treated mice were dose dependent. The number of neutrophils in BALF at the 0.2mg level was parallel to the content of ß-glucan in each particle. The numbers of lymphocytes and eosinophils in BALF at the 0.2mg level were parallel to the concentration of SO(4)(2-) in each particle. Pro-inflammatory mediators-such as interleukin (IL)-12, tumor necrosis factor-(TNF)-α, keratinocyte chemoattractant (KC), monocyte chemotactic protein (MCP)-l and macrophage inflammatory protein-(MIP)-lα in BALF-were greater in the treated mice. Specifically, NAD considerably increased pro-inflammatory mediators at a 0.2mg dose. The increased amounts of MlP-lα and TNF-α at 0.2mg dose corresponded to the amount of ß-glucan in each particle. The amounts of MCP-l or IL-12 corresponded to the concentration of sulfate (SO(4)(2-)) at a 0.2mg dose. These results suggest that inflammatory lung injury was mediated by ß-glucan or SO(4)(2-), which was adsorbed into the particles, via the expression of these pro-inflammatory mediators. The results also suggest that the variations in the magnitude of inflammation of the tested Kosa samples depend on the amounts of these toxic materials.